Neurocircuity of eating disorders

Abstract

Objectives: This chapter reviews brain imaging findings in anorexia and bulimia nervosa which characterize brain circuitry that may contribute to the pathophysiology of eating disorders (EDs).

Summary of recent findings: Recent imaging studies provide evidence of disturbed gustatory processing in EDs which involve the anterior insula as well as striatal regions. These results raise the possibility that individuals with anorexia nervosa have altered appetitive mechanism that may involve sensory, interoceptive, or reward processes. Furthermore, evidence of altered reward mechanisms is supported by studies that suggest that individuals with anorexia nervosa and bulimia nervosa share a trait toward similar anterior ventral striatal pathway dysregulation. This shared trait disturbance of the modulation of reward and emotionality may create a vulnerability for dysregulated appetitive behaviors. However, those with anorexia nervosa may be able to inhibit appetite and have extraordinary self-control because of exaggerated dorsal cognitive circuit function, whereas individuals with bulimia nervosa are vulnerable to overeating when they get hungry, because they have less ability to control their impulses.

Future directions: Current therapeutic interventions have modest success. Better understanding of neurocircuits that may be related to altered appetite, mood, impulse control, and other symptoms underlying the pathophysiology of EDs might improve psychotherapeutic and drug treatment strategies.

Fig. 1. Schematic of cortical–striatal pathways with a focus on taste

Chemoreceptors on the tongue detect a sweet taste. The signal is then transmitted through brainstem and thalamic taste centers to the primary gustatory cortex, which lies adjacent to and is densely interconnected with the anterior insula (AI). The AI is an integral part of the “ventral (limbic) neurocircuit” through its connections with the amygdala, the anterior cingulate cortex, and the orbitofrontal cortex. Afferents from the cortical structures involved in the ventral neurocircuit (AI and interconnected limbic cortices) are directed to the ventral striatum, whereas cortical structures involved in cognitive strategies (the dorsal neurocircuits) send inputs to the dorsolateral striatum. Thus, the sensory aspects of taste are primarily an insula phenomenon, whereas higher cortical areas modulate pleasure, motivation, and cognitive aspects of taste. These aspects are then integrated, resulting in an “eat” or “don’t eat” decision. Coding the awareness of pleasant sensation from the taste experience via the AI might be altered in AN patients, tipping the balance of striatal processes away from normal, automatic reward responses mediated by the ventral striatum and toward a more “strategic” approach mediated by the dorsal striatum. The figure links each cortical structure with similarly colored arrows, indicating all cortical structures project to striatum in topographic manner. ACC anterior cingulate cortex; DLPFC dorsolateral prefrontal cortex; NTS nucleus tractus solitarius; OFC orbitofrontal cortex